ArticleInfection and immunity2008
The absence of cutaneous lymph nodes results in a Th2 response and increased susceptibility to Leishmania major infection in mice.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- The proteinase-activated receptor-2 mediates protective immunity in early experimental leishmaniasis.Emerging microbes & infections · 2026Article
- LTβR deficiency causes lymph node aplasia and impaired B cell differentiation.Science immunology · 2024Article
- Construction of lymph nodes-targeting tumor vaccines by using the principle of DNA base complementary pairing to enhance anti-tumor cellular immune response.Journal of nanobiotechnology · 2024Article
- Immune Responses in Leishmaniasis: An Overview.Tropical medicine and infectious disease · 2022Review
- Aryl Hydrocarbon Receptor-Signaling Regulates EarlyFrontiers in immunology · 2019Article
- T cell-derived lymphotoxin limits Th1 response during HSV-1 infection.Scientific reports · 2018Article
- The LymphotoxinMediators of inflammation · 2017Article
- Association of prevalence of rhinitis, atopic eczema, rhinoconjunctivitis and wheezing with mortality from infectious diseases and with antibiotic susceptibility at a country level.Asia Pacific allergy · 2015Article
- Article
- Linking the microbiota and metabolic disease with lymphotoxin.International immunology · 2013Review
- Lymphotoxin signalling in immune homeostasis and the control of microorganisms.Nature reviews. Immunology · 2013Review
- Lymph node hypertrophy following Leishmania major infection is dependent on TLR9.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Role of the gut-associated and secondary lymphoid tissue in the induction of chronic colitis.Inflammatory bowel diseases · 2011Article
- Pulmonary responses to Stachybotrys chartarum and its toxins: mouse strain affects clearance and macrophage cytotoxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
- Keratinocytes determine Th1 immunity during early experimental leishmaniasis.PLoS pathogens · 2010Article
- Role of secondary lymphoid tissues in primary and memory T-cell responses to a transplanted organ.Transplantation reviews (Orlando, Fla.) · 2010Review
- PPEF/PP7 protein Ser/Thr phosphatases.Cellular and molecular life sciences : CMLS · 2009Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Lymph nodes (LNs) are important sentinel organs where antigen-presenting cells interact with T cells to induce adaptive immune responses. In cutaneous infection of mice with Leishmania major, resistance depends on the induction of a T-helper-cell-1 (Th1)-mediated cellular immune response in draining, peripheral LNs. We investigated whether draining, peripheral LNs are absolutely required for resistance against L. major infection. We investigated the course of experimental leishmaniasis in wild-type (wt) mice lacking peripheral LNs (pLNs), which we generated by in utero blockade of membrane-bound lymphotoxin, and in mice lacking pLNs or all LNs due to genetic deletion of lymphotoxin ligands or receptors. wt mice of the resistant C57BL/6 strain without local skin-draining LNs were still able to generate specific T-cell responses, but this yielded Th2 cells. This switch to a Th2 response resulted in severe systemic infection. We also confirmed these results with mice lacking pLNs due to genetic depletion of lymphotoxin-beta. The complete absence of LNs due to a genetic depletion of the lymphotoxin-beta receptor also resulted in a marked deterioration of disease and a Th2 response. Thus, in the absence of pLNs, an L. major-specific Th2 response is induced in the remaining secondary lymphoid organs, such as the spleen and non-skin-draining LNs. This indicates a critical requirement for pLNs to induce protective Th1 immunity and suggests that whether Th1 or Th2 priming to the same antigen occurs depends on the site of the primary antigen recognition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.